ArticleMolecular metabolism2026
Adiponectin preserves follicles through ADIPOR1/ADIPOR2-driven fatty acid metabolism.
Article in Molecular metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAdiponectin is a key regulator of glucose and lipid metabolism that improves insulin sensitivity and promotes mitochondrial fatty acid oxidation via ADIPOR1 and ADIPOR2. Ovarian lipid accumulation contributes to metabolic reproductive disorders such as polycystic ovary syndrome (PCOS), yet current hormone-based therapies have limited efficacy and potential adverse effects. We evaluated whether placenta-derived mesenchymal stem cells (PDMSCs) mitigate ovarian lipotoxicity by restoring adiponectin signaling.
methodsA thioacetamide (TAA) induced rat model of metabolic dysfunction with ovarian lipotoxicity was treated by intravenous transplantation of PDMSCs (2 × 10
resultsPDMSCs transplantation improved systemic insulin resistance and dyslipidemia and partially restored hepatic and ovarian architecture. PDMSCs treatment increased circulating and ovarian ADIPONECTIN levels and upregulated Adipor1/2 in ovarian tissue, accompanied by activation of the ADIPOR1/2/Fatty acid driven axis and enhanced mitochondrial fatty acid oxidation. These changes were associated with reduced ovarian lipid accumulation and improved endocrine homeostasis, including normalization of anti-Müllerian hormone (AMH), estradiol, and androgen levels, preservation of the primordial follicle pool, and induction of BMP15 expression. In vitro ADIPOR1/2 silencing abrogated these protective effects, supporting a requirement for adiponectin receptor signaling.
conclusionsPDMSCs ameliorate systemic and ovarian metabolic dysfunction in a TAA-induced model, consistent with adiponectin, ADIPOR1/2 dependent mitochondrial metabolic reprogramming. PDMSCs restore both metabolic and reproductive competence in the context of hepatic-ovarian metabolic crosstalk. These findings support PDMSC-based therapy as a mechanistically informed, multi-target strategy for the treatment of PCOS and metabolic-associated ovarian dysfunction.
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